Title : Aberrant activation of AMP-activated protein kinase remodels metabolic network in favor of cardiac glycogen storage.

Pub. Date : 2007 May

PMID : 17431505






4 Functional Relationships(s)
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1 Mutation of the gamma2 regulatory subunit of AMPK in humans renders the kinase insensitive to energy status and causes glycogen storage cardiomyopathy via unknown mechanisms. Glycogen gamma-aminobutyric acid (GABA) A receptor, subunit gamma 2 Mus musculus
2 Using transgenic mice expressing one of the mutant gamma2 subunits (N488I) in the heart, we found that aberrant high activity of AMPK in the absence of energy deficit caused extensive remodeling of the substrate metabolism pathways to accommodate increases in both glucose uptake and fatty acid oxidation in the hearts of gamma2 mutant mice via distinct, yet synergistic mechanisms resulting in selective fuel storage as glycogen. Glucose gamma-aminobutyric acid (GABA) A receptor, subunit gamma 2 Mus musculus
3 Using transgenic mice expressing one of the mutant gamma2 subunits (N488I) in the heart, we found that aberrant high activity of AMPK in the absence of energy deficit caused extensive remodeling of the substrate metabolism pathways to accommodate increases in both glucose uptake and fatty acid oxidation in the hearts of gamma2 mutant mice via distinct, yet synergistic mechanisms resulting in selective fuel storage as glycogen. Fatty Acids gamma-aminobutyric acid (GABA) A receptor, subunit gamma 2 Mus musculus
4 Using transgenic mice expressing one of the mutant gamma2 subunits (N488I) in the heart, we found that aberrant high activity of AMPK in the absence of energy deficit caused extensive remodeling of the substrate metabolism pathways to accommodate increases in both glucose uptake and fatty acid oxidation in the hearts of gamma2 mutant mice via distinct, yet synergistic mechanisms resulting in selective fuel storage as glycogen. Glycogen gamma-aminobutyric acid (GABA) A receptor, subunit gamma 2 Mus musculus